CV Physiology | Venous Return - Hemodynamics
Blood pressure may be measured in capillaries and veins, as well as the vessels Pulse can be palpated manually by placing the tips of the fingers across an . The relationship between blood volume, blood pressure, and blood flow is intuitively obvious. .. Thus, venoconstriction increases the return of blood to the heart. Venous return is the rate of blood flow back to the heart. It normally limits cardiac output. Although the above relationship is true for the hemodynamic factors that determine the flow of blood from the veins back to the heart, it is important not to. Under steady-state conditions, venous return must equal cardiac output (CO) when Although the above relationship is true for the hemodynamic factors that .
Several sites in the vascular system have large reservoir capacities. Portions of the vascular system have a large capacitance, that is, they can gain or lose large volumes of blood with little change in pressure. Therefore, as pressure within other portions of the venous system increases or decreases, large volumes of blood can move into or out of these reservoirs, buffering changes in pressure throughout the vascular system.
Smooth muscle of the vascular walls of some of the vessels in these sites can contract in response to sympathetic stimulation and circulating vasoconstrictor substances, significantly decreasing their capacitance and causing additional blood to be translocated to other portions of the circulation.
Large veins in the abdomen and thorax are especially effective reservoirs, as are the sinuses of the spleen and liver. The vascular plexuses of the skin can also function as reservoirs.
Blood flow into the skin is highly responsive to catecholamines released from the sympathetic nerves innervating the resistance vessels of the skin, the constriction of which decreases blood volume stored in the veins of the skin.
All of these reservoir functions can significantly affect mean systemic pressure, as their effective capacitance is altered, and blood is transferred to or from other portions of the vascular system. The vasopressor hormone angiotensin II is implicated as a causative factor in many forms of hypertension.
The renal sodium-retaining effects of angiotensin II are the primary mechanisms contributing to sustained blood pressure elevation, although the peptide has other significant vascular actions. Its effects on mean systemic pressure were analyzed in a series of studies in dogs in which angiotensin II was infused intravenously for 7 days, raising mean arterial blood pressure from the normal level of to mm Hg [ 5 ].
Blood volume remained unchanged, while mean systemic pressure rose from 9. The effect of the hormone was to increase the vascular tone, causing an increase in filling pressure at a constant blood volume. Right atrial pressure is normally approximately 0 mm Hg or atmospheric pressure. At a normal level of right atrial pressure, venous return will be normal as long as mean systemic pressure and resistance are normal.
Each additional 1 mm Hg increase resulted in a similar decrease in venous return, until atrial pressure reached 7 mm Hg, the mean systemic pressure, at which point flow into the heart ceased. The results of their study are plotted in Figure 2. As atrial pressure is raised from the normal value of 0 to 7 mm Hg, venous return falls from the normal level to 0.
The slope of the relationship is the inverse of the more When right atrial pressure is reduced below the normal value of 0 mm Hg, a different venous return response pattern is observed. But with subsequent 1 mm Hg increments in pressure reduction, the rate of rise in venous return falls progressively less until it reaches a steady level at pressures below —4 mm Hg. Further right atrial pressure reductions below —4 mm Hg will not increase venous return further.
The negative right atrial pressure and venous return data are presented in Figure 2. The relationship becomes curved as pressure falls to approximately —2 to —3 mm Hg as the slope decreases progressively with additional reductions in atrial pressure.
At approximately —4 mm Hg, the slope becomes 0, and further reductions do not cause additional increases in venous return. The relationship is curvilinear between —2 and —4 mm Hg due to progressively increasing resistance to venous return resulting from collapse of more The explanation for the nonlinear nature of the relationship in the negative pressure range of the right atrial pressure and the plateau below —4 mm Hg is the progressive collapse of veins as the luminal pressure falls below extramural pressure.
Within the chest, the pressure averages approximately —4 mm Hg but cycles between values more negative during inspiration to slightly positive during expiration.
As right atrial pressure, which is equal to venous pressure anywhere within the thorax, falls below atmospheric pressure, some veins just outside their point of entry into the thorax may collapse during inspiration, as their intraluminal pressure falls below atmospheric pressure. As central venous pressure falls lower, more veins may collapse for longer portions of the respiratory cycle, while below —4 mm Hg, essentially, all veins in the chest remain collapsed until the buildup of upstream blood increases their intraluminal pressure to —4 mm Hg or greater.
The collapse of the veins increases resistance to venous return, which is the inverse of the slope of the relationship between flow and right atrial pressure. Ultimately, resistance becomes infinite below —4 mm Hg, preventing any increase in flow above that present at —4 mm Hg. The resistance increases progressively as right atrial pressure falls from approximately —2 to —4 mm Hg, causing the plotted relationship between pressure and flow to be curvilinear in this range.
The pulsations of the right atrium cause a retrograde pressure wave that may progress through the central veins to varying distances. These pulses contribute to the fluctuations in venous closure that occur in the negative right atrial pressure range that are reflected in the curve or splay of the pressure—flow relationship. Changes in arterial as well as venous resistances affect venous return.
In Chapter 1the progressive blood pressure reductions throughout the vascular system were presented in Table 1.
Venous Return - Hemodynamics
The greatest segmental pressure reduction occurs at the arterioles, indicating that arterioles contribute the largest portion of total systemic vascular resistance.
Furthermore, the resistance of the arterioles is highly dynamic, capable of increasing or decreasing several folds in a few seconds. The smooth muscle in the arteriole walls responds rapidly to changes in concentrations of circulating vasoactive hormones, local metabolically linked mediators, and input from fibers of the sympathetic nervous system. Angiotensin II and catecholamines in the blood and locally produced endothelin are powerful arteriolar smooth muscle agonists, significantly affecting resistance to venous return.
In the experiment referred to above, in which angiotensin II was infused into dogs for 7 days, venous return remained unchanged while mean systemic pressure increased from 9. During this period, right atrial pressure increased slightly from 1.
Calculating resistance to venous return during the control period from the pressure gradient for venous return mean systemic pressure—right atrial pressure and the rate of venous return cardiac output yields a value of 2. After 7 days of angiotensin infusion, resistance to venous return increased to 3.
In a study on dogs, after a 7-day control period, angiotensin II was infused intravenously for an additional 7 days. Locally produced and circulating nitric oxide, prostacyclin, and prostaglandin E2 are vascular smooth muscle antagonists, producing arteriolar dilation and reduction of resistance to venous return.
Venous return curve - Wikipedia
Local tissue metabolism, in particular, aerobic metabolism, strongly affects arteriolar resistance. Activity that reduces tissue pO2 especially elicits significant arteriolar dilation and reduction in resistance to venous return.
The linkage between total body tissue oxygen demand and resistance to venous return is a fundamental mechanism governing control of cardiac output.
This is the basic mechanism by which the cardiovascular system responds to changes in demand for cardiac output as metabolic rate changes. Other means of cardiovascular control may take part in responses to metabolic changes, but this connection of tissue oxygen demand to resistance to venous return is of overriding significance. Oxygen demand is a strong determinant of resistance to venous return over periods ranging from seconds to hours and in long-term and steady-state conditions.
If demand is elevated for extended periods of days or weeks, new microvascular vessels grow through the tissue in need, decreasing local vascular resistance and increasing blood flow.
Conversely, if blood flow exceeds demand for periods of several days or more, microvascular vessels will degenerate, reducing vascular density and increasing resistance. This process is termed rarifaction and normally normally takes place in tissues whose use and metabolic activity are reduced.
Rarifaction also may occur if arterial blood pressure increases. For example, in the angiotensin II infusion experiment, the infusion resulted in a steady-state increase in arterial blood pressure of 60 mm Hg by affecting renal function, and the peptide had an immediate direct constrictor effect on the arterioles throughout the body.
Unsourced material may be challenged and removed. October Venous return is the rate of blood flow back to the heart. It normally limits cardiac output. Superposition of the cardiac function curve and venous return curve is used in one hemodynamic model. Under steady-state conditions, venous return must equal cardiac output Qwhen averaged over time because the cardiovascular system is essentially a closed loop.
Venous return curve
Otherwise, blood would accumulate in either the systemic or pulmonary circulations. Although cardiac output and venous return are interdependent, each can be independently regulated.
The circulatory system is made up of two circulations pulmonary and systemic situated in series between the right ventricle RV and left ventricle LV. Balance is achieved, in large part, by the Frank—Starling mechanism. For example, if systemic venous return is suddenly increased e. The left ventricle experiences an increase in pulmonary venous return, which in turn increases left ventricular preload and stroke volume by the Frank—Starling mechanism.
In this way, an increase in venous return to the heart leads to an equivalent increase in cardiac output to the systemic circulation. Therefore, increased venous pressure or decreased right atrial pressure, or decreased venous resistance leads to an increase in venous return.
PRA is normally very low fluctuating a few mmHg around a mean of 0 mmHg and PV in peripheral veins when the body is supine is only a few mmHg higher. Because of this, small changes of only a few mmHg pressure in either PV or PRA can cause a large percent change in the pressure gradient, and therefore significantly alter the return of blood to the right atrium.
For example, during lung expansion inspirationPRA can transiently fall by several mmHg, whereas the PV in the abdominal compartment may increase by a few mmHg. These changes result in a large increase in the pressure gradient driving venous return from the peripheral circulation to the right atrium.Cardiovascular - Cardiac Output - Frank Starling's Law
Therefore, one could just as well say that venous return is determined by the mean aortic pressure minus the mean right atrial pressure, divided by the resistance of the entire systemic circulation i. There is much confusion about the pressure gradient that determines venous return largely because of different conceptual models that are used to describe venous return.